Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.44 (AGT)
 770 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aim of the study was to investigate association of gene candidate polymorphisms encoding elements of the renin-angiotensin system and participating in regulation of vascular tone with development of microalbuminuria in patients with hypertensive disease. We examined 93 patients (52 women, 41 men, mean age 58.3+/-1.12 years, mean duration of hypertension 15.6+/-1.16 years) with hypertensive disease. Two patients had arterial hypertension (AG) with I, 22 with II, 63 with III degree of blood pressure (BP) elevation. Thirty four patients smoked, 2 had stroke in anamnesis, 33 had ischemic heart disease, in 58 heredity burdened with cardiovascular diseases was noted. In 38 patients hypertrophy of left ventricular myocardium was revealed. As gene-candidates we considered AGT, ACE, AT2R1, CYP11B2, MTHFR, PPARA, PPARG2, NOS3. Patients with microalbuminuria had significantly higher systolic and diastolic BP levels. Groups did not differ significantly according sex, age, disease duration, glucose level. There were no significant differences in involvement of other target organs - hypertrophy of left ventricular myocardium and atherosclerosis of carotid arteries. Patients with microalbuminuria had significantly higher level of blood cholesterol. Patients with and without microalbuminuria differed only in frequencies of genotypes of polymorphic marker A(-153)G of AT2R1 gene. Genotype AA predisposed to development of nephropathy--odds ratio (OR) 4.71 (95CI 1.78-12.97), while genotype AG was protective (OR 0.20 95%CI 0.07 to 0.56, p=0.031). According to results of multifactorial analysis independent factors affecting increase of risk of development of nephropathy in the studied group were level of systolic BP and carriage of genotype AA of polymorphic marker A(-153)G of AT2R1 gene.
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PMID:[Genetic aspects of development of microalbuminuria in patients with hypertensive disease]. 1907 77

With the aim to investigate association of polymorphisms of candidate genes with clinical peculiarities of hypertensive disease in patients having burdened familial anamnesis we examined 413 (229 men and 184 women, mean age 60.3 +/- 0.59 years) patients with essential arterial hypertension (AH). Determination of alleles and genotypes of polymorphic markers of ACE, AGT, AT2R1, CYP11B2, NOS3, ENDl, GNB3, PPARA, PPARG2, MTHFR, CAT, SOD2, PON1, PON2 sigma APOB, APOE, LPL genes was carried out with the use of polymerase chain reaction. Patient with AH having hereditary load were younger (58.9 +/- 0.75 and 61.3 +/- 0.89 years, respectively, p=0.017) and had significantly lower age of debut of the disease (44.4 +/- 0.84 and 47.5 +/- 1.03 years, respectively; p=0.013), higher values of systolic (204.8 +/- 7.66 and 187.0 +/- 2.04 mm Hg; p=0.032) and diastolic (111.2 +/- 1.05 and 107.3 +/- 1.17 mm Hg, respectively; p=0.025) arterial pressure (AP) compared with patients with AH without hereditary loaded anamnesis. Portion of patients with 3 degree of severity of AH was higher among patients with "familial" AH (53.6 and 44.1%, respectively, p=0.018). Early debut (in the age younger than 45 years in men and 55 years in women) was associated with carriage of genotype TT of polymorphic marker C825 of GNB3 gene (OR 2.65 95CI [1.27-5.54], p=0.005) and genotype AA of polymorphic marker A(A153)G of AT2R1 gene (OR 1.67 95% CI [1.03-2.77], p=0.024). Higher AP level corresponding to 3-rd degree AH in the group of patients with burdened familial anamnesis was associated with carriage of Asn allele of polymorphic marker Lysl98Asn of EDN1 gene (OR 2.24 95% CI [1.20-4.18], p=0.008), 4a allele of polymorphic marker 4a/4b of NOS3 gene (OR 2.23 C/[1.29-3.83], p=0.002), genotype ArgArg of polymorphic marker Glnl92Arg of PON1 gene (OR 6.14 C7[1.46-25.67], p=0.01), T allele of polymorphic marker of C825T gene GNB3 (OR 1.75 C/[1.11-2.76], p=0.01) and genotype AA of polymorphic marker A(A153)G of AT2R1 gene (OR 2.61 C/11.29-5.34], p=0.005). In patients without burdened familial anamnesis 3-rd degree AH was associated with higher frequency of allele Ala of polymorphic marker Pro12A1a of PPARG2 gene.
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PMID:[Association of genetic factors with clinical peculiarities of hypertensive disease in patients with burdened familial anamnesis]. 1925 15

The Inuit population is often described as being protected against CVD due to their traditional dietary patterns and their unique genetic background. The objective of the present study was to examine gene-diet interaction effects on plasma lipid levels in the Inuit population. Data from the Qanuippitaa Nunavik Health Survey (n 553) were analysed via regression models which included the following: genotypes for thirty-five known polymorphisms (SNP) from twenty genes related to lipid metabolism; dietary fat intake including total fat (TotFat) and saturated fat (SatFat) estimated from a FFQ; plasma lipid levels, namely total cholesterol (TC), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C) and TAG. The results demonstrate that allele frequencies were different in the Inuit population compared with the Caucasian population. Further, seven SNP (APOA1 - 75G/A (rs670), APOB XbAI (rs693), AGT M235T (rs699), LIPC 480C/T (rs1800588), APOA1 84T/C (rs5070), PPARG2 - 618C/G (rs10865710) and APOE 219G/T (rs405509)) in interaction with TotFat and SatFat were significantly associated with one or two plasma lipid parameters. Another four SNP (APOC3 3238C>G (rs5128), CETP I405V (rs5882), CYP1A1 A4889G (rs1048943) and ABCA1 Arg219Lys (rs2230806)) in interaction with either TotFat or SatFat intake were significantly associated with one plasma lipid variable. Further, an additive effect of these SNP in interaction with TotFat or SatFat intake was significantly associated with higher TC, LDL-C or TAG levels, as well as with lower HDL-C levels. In conclusion, the present study supports the notion that gene-diet interactions play an important role in modifying plasma lipid levels in the Inuit population.
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PMID:Gene-diet interactions on plasma lipid levels in the Inuit population. 2302 45